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1 activity (determined using A(1)AR or A(3)AR null mice).
2 -wounding but are completely absent in TSG-6-null mice.
3 also observed in nonobese wild-type and LepR-null mice.
4 Syn1 and Bdnf in the embryonic brain of Arx-null mice.
5 emperature in wild-type mice but not in Opn5-null mice.
6 ynia in female WT mice, but not in the HCAR2-null mice.
7 h human and mouse platelets but not in PTPN7-null mice.
8 he dystrophic phenotype in alpha-sarcoglycan-null mice.
9 However, some loci are unaffected in Zfp57-null mice.
10 gene expression in PPK-like lesions of Krt16-null mice.
11 itive neutrophils was transferrable to OLFM4 null mice.
12 xybutyrate (BHB) in wild-type (WT) and HCAR2-null mice.
13 d on OL progenitor cells purified from Thap1 null mice.
14 eased rate of arrhythmia in heterozygous and null mice.
15 -type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice.
16 econstitute the vascular dysfunction in CD36-null mice.
17 ce but are profoundly impaired in BK channel-null mice.
18 of Whsc1 prevented tumor progression in PTEN-null mice.
19 PPARgamma suppression causes alopecia in VDR-null mice.
20 icantly increased in Mybphl heterozygous and null mice.
21 autophagy inhibition is attenuated in FGF15-null mice.
22 del of CKD-mineral bone disorder and alphaKL-null mice.
23 gets and in genes upregulated in miR-132/212 null mice.
24 e in the lung of wildtype but not caveolin-1-null mice.
25 th increased metastasis as compared with p53-null mice.
26 in (AG) and UAG were abolished in male GHS-R-null mice.
27 CYP2A13/2F1-humanized mice than in Cyp2abfgs-null mice.
28 the exaggerated fibrosis observed in Twist1-null mice.
29 lial-to-mesenchymal transition (EMT) in Pten-null mice.
30 ng persistent DNA damage in p53R172H and p53-null mice.
31 were measured in 16HBE cells and claudin-18 null mice.
32 ked the defective hypoxic responses of Epas1-null mice.
33 tagonist or is completely abolished in Trpv1 null mice.
34 reviously reported for Rnaseh2b- or Rnaseh2c-null mice.
35 le acid metabolism was also evident in Gpat3-null mice.
36 tion compensates for PKMzeta loss in PKMzeta-null mice.
37 ol6a2Deltaex5 mice than in gamma-sarcoglycan-null mice.
38 nt or at the onset of RTT phenotype in Mecp2-null mice.
39 eletal muscle pathology in gamma-sarcoglycan-null mice.
40 btained from the developing calvaria of DSPP-null mice.
41 ge was seen among matrix metalloproteinase-8 null mice.
42 rginally higher compared with Akita and Ncf1 null mice.
43 ntagonist reduced ileal inflammation in SHIP-null mice.
44 ent, that were significantly induced in PGRN null mice.
45 esis, we crossed DYT1 knock-in with p58(IPK)-null mice.
46 mammary fat pad of wild-type mice and Gpr81-null mice.
47 expression in the cortex of WT but not MMP-9-null mice.
48 wide expression of mutant ATXN1 and in ATXN1 null mice.
49 4.1B and betaII spectrin expression in Caspr-null mice.
50 rements confirm a thermogenic defect in NCLX-null mice.
51 ed adipose tissue lipid mobilization in CT-1 null mice.
52 is genes FASN and ACC1 is impaired in IQGAP1-null mice.
53 nction of this receptor in vivo using Jedi-1 null mice.
54 tion deficits observed in the Neurexophilin4 null mice.
55 similar to the protection observed in SARM1-null mice.
56 letal phenotypes similar to those of Cyp27b1-null mice.
57 adiponectin null mice, but not in T-cadherin null mice.
58 ficit or the cochlear abnormalities of BACE1 null mice.
59 type animals, but not in the retina of GPR81-null mice.
60 posure also was observed in the AM from RAGE null mice.
61 enotype seen in the cerebral cortex of Vldlr(null) mice.
62 in WT versus paranode defective (i.e., Caspr-null) mice.
63 ut not purified immunoglobulin, into obese B(null) mice.
64 ) (ATP binding cassette subfamily B member 4 null) mice.
67 crossed Idh1-KI mice with conditional Trp53 null mice, a well-characterized model of T-cell malignan
68 This effect was completely lost in the HCAR2-null mice after a 2-d starvation protocol, in which the
71 or initiated, and consistent with this LRBA-null mice also demonstrate resistance to lethal GvHD.
75 omain of CIZ1 and the E repeats of Xist CIZ1-null mice, although viable, display fully penetrant fema
79 the in vivo role of RTN1, we generated RTN1-null mice and compared the effects of RTN1 and RTN3 on B
81 explain the parturition differences in Cox-1 null mice and gestation-matched wild type (WT) controls.
83 t patterns downstream of single cones in Bax null mice and may serve to maintain constancy in both th
84 A and completely rescue both survival of Smn null mice and motor neuron electrophysiology demonstrati
85 ophages from heme overload in heme-loaded Hx-null mice and reduces production of cytokines and reacti
86 we investigated the bone phenotype in Bmpr1b null mice and the impacts of loss of Bmpr1b on osteoblas
87 By using intravital microscopy with DREAM-null mice and their bone marrow chimeras, we demonstrate
89 y higher tumorigenesis in NOD/Scid/IL2Rgamma-null mice, and immunostaining of mouse CD31 revealed tha
92 t from being prone to tumor development, Arf-null mice are blind, and their male germ cells exhibit d
104 display a reduced fetal size, whereas PRMT6 null mice are viable, which permits the generation of do
106 duced G protein activation are seen in RGS12-null mice, as well as enhanced sensitivity to KOR agonis
108 hmt (betaine-homocysteine methyltransferase)-null mice at age 4, 12, 24, and 52 wk (N = 8) and observ
111 In contrast, macrophages from ACE knockout (null) mice averaged only 28% of the ATP levels found in
113 Lastly, mRNA from tuberous sclerosis-1/2-null mice brain tissue exhibiting ER stress had increase
117 t delay in AML progression in NOD/SCID/IL2Rg(null) mice, but the persistence of adoptively transferre
119 Patients who lack PLP1 expression, and Plp1-null mice, can display comparatively mild phenotypes, su
121 ity, were significantly increased in nAChRa7 null mice (Chrna7(-/-)) relative to wild-type mice.
126 of cell death in intestinal tissue of cIAP1-null mice, compared with wild-type C57BL/6 mice, cIAP2-n
127 e mTert gene in the first generation of Tert null mice compromised tumor growth, with reduced VEGF ex
130 cells are significantly reduced in CysLT(2)R-null mice (Cysltr2 (-/-)) compared with WT and CysLT(1)R
131 of IgG was studied using IgG mu heavy chain-null mice deficient in mature B cells and by IgG transfe
132 Ldlr(-/-) (low-density lipoprotein receptor null) mice deficient in miR-146a develop less atheroscle
137 gest attenuated oxidative stress in the RAGE null mice despite comparable CS exposure and lung leukoc
140 -null and haematopoietic hypocretin-receptor-null mice develop monocytosis and accelerated atheroscle
144 our previous studies, we showed that Trim32 null mice developed Th2-biased skin inflammation in resp
150 fects, cortical pyramidal neurons from Upf3b-null mice display deficient dendritic spine maturation i
153 ort that mice lacking Nogo receptors (NgR123-null mice) display complete CC agenesis due to axon misd
156 ly, tumors growing in C/EBPalpha conditional null mice displayed greater MDSC infiltration, increased
159 d macrophages (BMDMs) isolated from RORgamma-null mice displayed reduced capacity to secrete IL-1beta
162 y, expression of Mg29 in the hearts of Csrp3 null mice (encoding muscle LIM protein, MLP) partially r
163 sion only in GABAergic neurons of male Mecp2 null mice enhanced inhibitory signaling, extended lifesp
165 urrent is absent in cochlear cells of Piezo2-null mice, even though the normal MT current persists.
166 Independent studies have shown that Sox3 null mice exhibit a spermatogenic block as young adults,
171 nsistent with computational predictions, Id3-null mice exhibit increased numbers of cells expressing
172 oss of MyHC-emb function in vitro Adult Myh3 null mice exhibit scoliosis, a characteristic phenotype
174 static synaptic scaling [3-6], but TNF-alpha-null mice exhibited no apparent cognitive or emotional a
176 ly, in contrast to lamin A/C-null mice, SUN2-null mice fail to show coincident fibrosis or upregulati
177 Indirect calorimetry showed that Cyp2e1-null-mice fed FF exhibited consistently higher total ene
178 ls were cultured from wild-type and tryptase null mice, followed by an assessment of their profile of
180 advanced lung tumours from Kras(G12D/+);p53-null mice frequently exhibit Kras(G12D) allelic enrichme
182 Here, we find that in heterozygous gata3 null mice (gata3(+/-) ) outer hair cells (OHCs) differen
183 consistent with normal adipose mass in GPAT3-null mice, GPAT3 inhibition did not prevent the formatio
184 mice, whereas all WT mice survived, and Nrf2 null mice had a defect in clearance, particularly at the
193 In addition, neural stem cells from Upf3b-null mice have impaired ability to undergo differentiati
194 treated with anti-CD47 antibodies, and Cd47-null mice have impaired intestinal mucosal wound healing
197 ritical role in mammary gland function; ZnT2-null mice have profound defects in mammary epithelial ce
202 ge cells; early embryonic lethality in Bag-1 null mice, however, has limited the investigation of BAG
204 ied evidence of partial lipoatrophy in Reep1 null mice in addition to prominent spastic paraparesis.
206 tudy was carried out with wild-type and CT-1 null mice in fed (ad libitum) and food-restricted condit
207 pR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol
208 ctive prostasin are viable, unlike prostasin null mice, indicating that at least some prostasin funct
209 nocyte and fibroblast migration in the Rhamm-null mice, indicating that RHAMM suppresses keratinocyte
210 evated in the developing tooth germ of Smad7 null mice, indicating the hyperactivation of the canonic
212 transplantation from platelet-specific ERK5 null mice into hyperlipidemic apolipoprotein E null mice
213 pite GC losses, retinal organization in Brn3 null mice is remarkably similar to that of wild-type con
214 ts from HFD-fed beta cell-specific Galpha(z)-null mice is significantly improved as compared with isl
215 n MDM2-ALT1 is ubiquitously expressed in p53 null mice it leads to increased incidence of spindle cel
216 We found that, unlike in WT mice, in Rhamm-null mice, keratinocyte migration initiates prematurely
217 or (VDR) only in the distal intestine of VDR null mice (KO/TG mice) results in the normalization of s
218 singly, damaged white matter tracts in Olig1-null mice lacked Olig2(+) OPCs, and instead proliferatin
219 docytopathy was completely preserved in MC1R-null mice, marked by reduced albuminuria and diminished
220 of pathology in dystrophic mice, dystrophin-null mice (mdx(betageo)) presented with a mildly exacerb
223 rmline liver fatty acid (FA) binding protein null mice (Mttp-LKO, i.e., double knockout mice) hepatic
224 cognitive impairment is not observed in tau-null mice or in mice treated with anti-tau antibodies, d
234 HSC aging and inflammation in young miR-146a-null mice, preceding development of aging-associated mye
235 tissues and intestinal macrophages from SHIP-null mice produced higher levels of IL1B and IL18 than i
236 imary tumor burden, Notch activation in Pten-null mice promoted epithelial-mesenchymal transition and
237 sfer experiments, matrix metalloproteinase-8 null mice receiving wild-type marrow had a survival adva
241 sively in the somatosensory neurons of Mecp2-null mice rescues tactile sensitivity, anxiety-like beha
242 on of specific DNA loci in the liver of Bhmt-null mice results in repression of Iqgap2 and F2rl2 and
243 )-induced premature senescence in caveolin-1-null mice results in the formation of more abundant lung
245 the fasting response in wild-type and IQGAP1-null mice revealed that transcriptional regulation of th
246 lysis of both male and female maternal Ube3a-null mice reveals that microcephaly in the AS mouse mode
253 ll mice into hyperlipidemic apolipoprotein E null mice showed decreased platelet accumulation and inc
254 g-term pressure overload both Atf6 and Atf6b null mice showed enhanced decompensation typified by inc
255 ively in OCs (CtskCreRor2 (fl/fl) ) in Sfrp4 null mice significantly reversed the increased number of
258 orotic phenotype that is very similar to opg-null mice, suggesting that the antiresorption activity o
260 ium-phosphate cotransporter Npt2a in alphaKL-null mice supporting direct actions of cKL in the absenc
261 s, we exploited humanized NOD-scid IL2rgamma(null) mice systemically infected with HIV-1 to generate
262 e to death was significantly faster in PTPN7-null mice than in WT mice in a pulmonary thromboembolism
264 ree different atherosclerosis models in ApoE null mice that prolonged systemic treatment with LyP-1 t
265 ted, streptozotocin-treated ghrelin receptor-null mice that were administered GcgR monoclonal antibod
268 Ldlr(-/-) (low-density lipoprotein receptor null) mice transplanted with bone marrow (BM) cells from
270 efects that rendered adipose-specific PGRMC2-null mice unable to activate adaptive thermogenesis and
271 human IL-2 to NSG -( K(b) D(b)) (null) ( IA(null)) mice via adeno-associated virus vector increased
272 r formation observed in p53(5KR/5KR) and p53-null mice was suppressed upon the treatment of the mTOR
273 eveloped in p53 wild-type ((+/+)) versus p53 null ((-/-)) mice, we observed higher GMPS expression in
274 intrathecal injection into 6-month-old Gjb1-null mice, we confirmed expression of Cx32 in lumbar roo
275 tor, nitrobenzylthioinosine (NBTI), and ENT1-null mice, we demonstrated that ENT blockade elevated lu
278 ased delta opioid receptor activity in Gpr88 null mice, we investigated the impact of GPR88 co-expres
285 elinated corpus callosum projections of Msh2-null mice were smaller than wild-type mice, whereas unmy
289 ysosomes in the gastric epithelium of trpml1-null mice, where they are protected from eradication the
290 an IgG clearance in NSG- B2M(null) ( IA IE) (null) mice whereas clearance in NSG -( K(b) D(b)) (null)
291 gly increased from 15 to 31 and 100% in Nrf2 null mice, whereas all WT mice survived, and Nrf2 null m
292 elay in the onset of prostate cancer in Pten-null mice, whereas Kdm5b loss alone caused no morphologi
293 n primary murine chondrocytes from A2AR(-/-) null mice, which develop spontaneous OA by 16 weeks, the
295 the complex pathological phenotypes of FUT8 null mice, which display defects in cellular signaling,
296 se to VRS using TRPV1 antagonism or in Trpv1 null mice while the response to passive stretch remains
297 ng hormone axons was reduced in adult Magel2-null mice, while the density of orexigenic agouti-relate
299 wed greater sensitivity to NA than Cyp2abfgs-null mice, with greater depletion of nonprotein sulfhydr